NEET-PG Dermatology Previous Year Questions (2017–2026)

Correct Answer: A. Tuberculoid leprosy with a positive lepromin test

Few hypopigmented anesthetic patches, a thickened tender nerve, and epithelioid granulomas with scant bacilli (paucibacillary) define tuberculoid leprosy. Strong cell-mediated immunity contains the bacilli but drives granulomatous damage, giving a positive lepromin test.

Solitary hypopigmented, anesthetic patch typical of paucibacillary (tuberculoid) leprosy.

Why the other options fail

• B and D. Lepromatous leprosy: shows multiple symmetric lesions, foamy macrophages loaded with bacilli (multibacillary), and defective CMI giving a negative lepromin test, not this picture.
• C. Erythema nodosum leprosum: is a Type III (immune complex) reaction seen in lepromatous/borderline lepromatous disease, presenting with tender red nodules and systemic symptoms, not this clinical picture.

Pearl: few lesions, thickened nerve, granulomas, positive lepromin -- tuberculoid leprosy, the high-immunity pole of the disease spectrum.

Correct Answer: A. Phrynoderma

Phrynoderma ("toad skin") is follicular hyperkeratosis on extensor surfaces (elbows, knees, buttocks), from a combined deficiency of essential fatty acids, B-complex vitamins, and vitamins A/C -- explaining its improvement with these nutrients.

Why the other options fail

• B. Kwashiorkor: shows edema, hepatomegaly, and "flaky paint" dermatosis, not follicular papules.Sparse, discolored hair and cheilosis in a child with kwashiorkor.
• C. Rickets: from vitamin D deficiency causes skeletal changes (craniotabes, rachitic rosary, bowed legs), not follicular skin lesions.
• D. Marasmus: causes severe muscle/fat wasting ("old man face"), not hyperkeratotic papules.

Pearl: "toad skin" follicular papules on extensor surfaces responding to vitamin A/C/EFA repletion is phrynoderma.

Correct Answer: C. Screen for underlying hyperandrogenism

Severe cystic acne resistant to both systemic antibiotics and a full course of oral isotretinoin in a woman should prompt evaluation for hyperandrogenism, since excess androgens directly drive sebum overproduction, fueling acne despite therapies that would otherwise be sufficient -- and raising suspicion for conditions like PCOS, especially with hirsutism or androgenetic alopecia.

Why the other options fail

• A. Review medication list for drug-induced acne: Worth considering generally, but less likely as the primary explanation for severe disease unresponsive even to isotretinoin without a specific triggering history.
• B. Bacterial culture for resistant strains: More relevant to antibiotic failure alone, but isotretinoin acts directly on sebaceous glands rather than bacteria, so its failure points elsewhere.
• D. Strict elimination diet: Lacks strong evidence as a primary driver of severe recalcitrant acne.

Pearl: Acne that survives a full isotretinoin course in a woman is a red flag for hormonal drive -- hyperandrogenism workup, not another round of antibiotics, is the next right step.